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Restrict the search for
ethanolamine oleate
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There is one exact (name or code) match for ethanolamine oleate
Status:
US Approved Rx
(1988)
Source:
NDA019357
(1988)
Source URL:
First approved in 1988
Source:
NDA019357
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Ethanolamine oleate is a salt of ethanolamine, a basic substance, and oleic acid. It is marketed under a trade name of Ethamoline as a sclerotic agent for the treatment of patients with esophageal varices that have recently bled, to prevent rebleeding. In vitro studies revealed that ethanolamine oleate inhibits fibrin clot formation because of the Ca2+-chelating ability of its constituent ethanolamine. Nevertheless, from in vivo studies it was suggested that intravascular injection of ethamoline activates the local coagulation system. The activation may be accelerated by an acute inflammatory process provoked by oleate, which is supported by such clinical manifestations as mild fever, retrosternal pain leukocytosis and an increase in plasma fibrinogen level.
Status:
US Approved Rx
(1988)
Source:
NDA019357
(1988)
Source URL:
First approved in 1988
Source:
NDA019357
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Ethanolamine oleate is a salt of ethanolamine, a basic substance, and oleic acid. It is marketed under a trade name of Ethamoline as a sclerotic agent for the treatment of patients with esophageal varices that have recently bled, to prevent rebleeding. In vitro studies revealed that ethanolamine oleate inhibits fibrin clot formation because of the Ca2+-chelating ability of its constituent ethanolamine. Nevertheless, from in vivo studies it was suggested that intravascular injection of ethamoline activates the local coagulation system. The activation may be accelerated by an acute inflammatory process provoked by oleate, which is supported by such clinical manifestations as mild fever, retrosternal pain leukocytosis and an increase in plasma fibrinogen level.
Status:
US Approved Rx
(2015)
Source:
ANDA204517
(2015)
Source URL:
First approved in 1972
Source:
FLUORINE F-18 by GE HEALTHCARE
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
FLUORIDE ION F-18 (as sodium fluoride F-18) is a radioactive diagnostic agent for positron emission tomography (PET) indicated for imaging of bone to define areas of altered osteogenic activity. FLUORIDE ION F-18 normally accumulates in the skeleton in an even fashion, with greater deposition in the axial skeleton (e.g. vertebrae and pelvis) than in the appendicular skeleton and greater deposition in the bones around joints than in the shafts of long bones. Increased FLUORIDE ION F-18 deposition in the bone can occur in areas of increased osteogenic activity during growth, infection, malignancy (primary or metastatic) following trauma, or inflammation of the bone.
Status:
US Approved Rx
(2022)
Source:
ANDA204934
(2022)
Source URL:
First marketed in 1937
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Niacin (also known as vitamin B3 and nicotinic acid) is bio converted to nicotinamide which is further converted to nicotinamide adenine dinucleotide (NAD+) and the hydride equivalent (NADH) which are coenzymes necessary for tissue metabolism, lipid metabolism, and glycogenolysis. Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and TC, and increases HDL-C. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). The mechanism by which niacin alters lipid profiles is not completely understood and may involve several actions, including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity (which may increase the rate of chylomicron triglyceride removal from plasma). Niacin decreases the rate of hepatic synthesis of VLDL-C and LDL-C, and does not appear to affect fecal excretion of fats, sterols, or bile acids. As an adjunct to diet, the efficacy of niacin and lovastatin in improving lipid profiles (either individually, or in combination with each other, or niacin in combination with other statins) for the treatment of dyslipidemia has been well documented. The effect of combined therapy with niacin and lovastatin on cardiovascular morbidity and mortality has not been determined. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear. April 15, 2016: Based on several large cardiovascular outcome trials including AIM-HIGH, ACCORD, and HPS2-THRIVE, the FDA decided that "scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events" Consistent with this conclusion, the FDA has determined that the benefits of niacin ER tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.
Status:
US Approved Rx
(2024)
Source:
ANDA216113
(2024)
Source URL:
First marketed in 1921
Source:
Copper Sulphate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Tetraamminecopper sulfate is a dark blue crystalline solid with a faint odor of ammonia. The primary hazard is the threat to the environment. Immediate steps should be taken to limit its spread to the environment. Used as a pesticide and fungicide, to print fabrics (especially in calico finishing), and to make other copper compounds.
Status:
US Approved Rx
(2009)
Source:
ANDA079139
(2009)
Source URL:
First marketed in 1921
Source:
Lithium Salicylate N.F.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and John Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.
Status:
US Approved Rx
(2013)
Source:
NDA204223
(2013)
Source URL:
First marketed in 1827
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Morphine is one of the most important and widely used opioid for the treatment of chronic and acute pain: the very wide interindividual variability in the patients’ response to the drug may have genetic derivations. Sulphate salt of morphine sold under the many brand names, one of them, DURAMORPH, which is indicated for the management of pain severe enough to require use of an opioid analgesic by intravenous administration, and for which alternative treatments are not expected to be adequate. In addition for the epidural or intrathecal management of pain without attendant loss of motor, sensory, or sympathetic function. Morphine is a full opioid agonist and is relatively selective for the mu-opioid receptor, although it can bind to other opioid receptors at higher doses. The principal therapeutic action of morphine is analgesia. Like all full opioid agonists, there is no ceiling effect for analgesia with morphine. The precise mechanism of the analgesic action is unknown. However, specific CNS opioid receptors for endogenous compounds with opioid-like activity have been identified throughout the brain and spinal cord and are thought to play a role in the analgesic effects of this drug. Morphine has a high potential for addiction and abuse. Common side effects include drowsiness, vomiting, and constipation. Caution is advised when used during pregnancy or breast-feeding, as morphine will affect the baby.
Status:
US Approved OTC
Source:
21 CFR 336.10(d) antiemetic meclizine hydrochloride
Source URL:
First approved in 1954
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Meclizine, a piperazine-derivative H1-receptor antagonist similar to buclizine, cyclizine, and hydroxyzine, is used as an antivertigo/antiemetic agent. Meclizine is used in the management of nausea, vomiting, and dizziness associated with motion sickness and vertigo in diseases affecting the vestibular apparatus. Along with its actions as an antagonist at H1-receptors, meclizine also possesses anticholinergic, central nervous system depressant, and local anesthetic effects. Meclizine depresses labyrinth excitability and vestibular stimulation and may affect the medullary chemoreceptor trigger zone. It is sold under the brand names Bonine, Bonamine, Antivert, Postafen, Sea Legs, and Dramamine II.
Status:
US Approved OTC
Source:
21 CFR 346.18(a) anorectal:astringent calamine
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
There is no available information related any biological and pharmaceutical application of ammonium tetrachlorozincate.
Status:
US Approved OTC
Source:
21 CFR 346.18(a) anorectal:astringent calamine
Source URL:
First marketed in 1921
Source:
Solution of Ferric Subsulphate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Ferric Ammonium EDTA Solution is normally used as a photographic chemical for a bleaching agent in the process of colour washing. It is also used as a complexing, and oxidizing agent & as a fertilizer and catalyst. EDTA acid are colourless, water-soluble solid that are widely used to dissolve scale. The usefulness of these ammonium salts arise because of its role as a chelating agent, i.e. its ability to "sequester" metal ions such as Ca2+ and Fe3+.
Status:
US Approved OTC
Source:
21 CFR 355.10(a)(2) anticaries:dentifrices sodium fluoride powder
Source URL:
First marketed in 1921
Source:
Calcium Chloride U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Olaflur (amine fluoride 297, trade name elmex gel) is a fluoride-containing substance that is an ingredient of toothpastes and solutions for the prevention of dental caries. Especially in combination with dectaflur, it is also used in the form of gels for the treatment of early stages of caries, sensitive teeth, and by dentists for the refluoridation of damaged tooth enamel. Olaflur is a salt consisting of an alkyl ammonium cation and fluoride as the counterion. With a long lipophilic hydrocarbon chain, the cation has surfactant properties. It forms a film layer on the surface of teeth, which facilitates incorporation of fluoride into the enamel. The top layers of the enamel's primary mineral, hydroxylapatite, are converted into the more robust fluorapatite. The fluoridation reaches only a depth of a few nanometres, which has raised doubts whether the mechanism really relies on the formation of fluorapatite.
